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Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men

Received: 11 December 2013     Published: 30 December 2013
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Abstract

Profuse epidemiological evidence supports a higher risk for coronary heart disease and stroke in smoker women than in men with the same habit. Although it is already known that cigarette smoking alters the redox state, is unknown if the imbalance in the normal equilibrium between oxidants and antioxidants is responsible for the elevated female susceptibility. Therefore, the aim of this work was to estimate the effect of smoking on serum redox status in women compared with men, accounting for divergences in other major risk factors for cardiovascular disease. Lipid profile, antioxidant capacity, and serum carbonyls were assessed in 116 healthy Uruguayans, composed by 50 females and 66 males. The smoking habit was declared by 17 females (34 %) and 36 males (54 %). The lipid profile was modified by cigarette smoking, affecting in a different way males and females. In particular, HDL-C that was higher in non-smoker females (59 (28) mg/dL) than in non-smoker males (46 (14) mg/dL) significantly decreased in smoker females (51 (13) mg/dL), remaining unchanged in the smoker male population (42 (12) mg/dL). Conversely LDL-C, which gave similar values for non-smoker females (110.1 ± 35.2 mg/dL) and males (98.5 ± 36.0 mg/dL), increased exclusively in smoker males (122.2 ± 36.4 mg/dL, p<0.05). In turn, the level of serum antioxidants that was higher in non-smoker males (1.9  0.3 mM FRAP) than females (1.5  0.4 mM /FRAP), remained unchanged in smokers. Similar results were obtained for carbonyls, which showed higher levels in non-smoker males (0.90 ± 0.32 nmol/mg of protein) than females (0.74 ± 0.32 nmol/mg of protein), and while the level remained unmodified in smokers males (0.86  0.28 nmol/mg of protein) increased non-significantly in smoker females (0.79  0.31 nmol/mg of protein). Whereas the oxidation index correlated positively with LDL-C (r = 0.45) in smoker males, and with triglycerides in both non-smoker and smoker females(r = 0.42 and 0.79, respectively), a negative and intense correlation with HDL-C (r = -0.79), and a positive one with the LDL-C/HDL-C index (r = 0.87) was observed exclusively in smoker females. Our results point to an association at the molecular level between oxidative stress footprints and plasma lipoprotein/cholesterol concentration predominantly in smoker females, and support the concept that the higher sensitivity of women to smoking related cardiovascular pathology is associated with oxidants-mediated biomolecular insults.

Published in American Journal of Clinical and Experimental Medicine (Volume 1, Issue 3)
DOI 10.11648/j.ajcem.20130103.13
Page(s) 53-57
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2013. Published by Science Publishing Group

Keywords

Cardiovascular Disease, Cigarette Smoking, Lipid Profile, Gender, Antioxidants, Protein Oxidation

References
[1] Stephens, J. W.; Gable, D. R.; Hurel, S. J.; Miller, G. J.; Cooper, J. A.; Humphries, S. E. Increased plasma markers of oxidative stress are associated with coronary heart disease in males with diabetes mellitus and with 10-year risk in a prospective sample of males. Clin Chem 52:446-452; 2006.
[2] Wang, J. C.; Bennett, M. Aging and atherosclerosis: mechanisms, functional consequences, and potential therapeutics for cellular senescence. Circ Res 111:245-259; 2012.
[3] Tobacco. Fact sheet No 339. WHO Media Centre; 2013.
[4] Huxley, R. R.; Woodward, M. Cigarette smoking as a risk factor for coronary heart disease in women compared with men: a systematic review and meta-analysis of prospective cohort studies. Lancet 378:1297-1305; 2011.
[5] Woodward, M.; Tunstall-Pedoe, H.; Smith, W. C.; Tavendale, R. Smoking characteristics and inhalation biochemistry in the Scottish population. J Clin Epidemiol 44:1405-1410; 1991.
[6] Parish, S.; Collins, R.; Peto, R.; Youngman, L.; Barton, J.; Jayne, K.; et al. Cigarette smoking, tar yields, and non-fatal myocardial infarction: 14,000 cases and 32,000 controls in the United Kingdom. The International Studies of Infarct Survival (ISIS) Collaborators. BMJ 311:471-477; 1995.
[7] McClave, A. K.; Hogue, C. J.; Brunner Huber, L. R.; Ehrlich, A. C. Cigarette smoking women of reproductive age who use oral contraceptives: results from the 2002 and 2004 behavioral risk factor surveillance systems. Women Health Issues 20:380-385; 2010.
[8] Hakim, I. A.; Harris, R.; Garland, L.; Cordova, C. A.; Mikhael, D. M.; Sherry Chow, H. H. Gender difference in systemic oxidative stress and antioxidant capacity in current and former heavy smokers. Cancer Epidemiol Biomarkers Prev 21:2193-2200; 2012.
[9] Rosello-Lleti, E.; de Burgos, F. G.; Morillas, P.; Cortes, R.; Martinez-Dolz, L.; Almenar, L.; et al. Impact of cardiovascular risk factors and inflammatory status on urinary 8-OHdG in essential hypertension. Am J Hypertens 25:236-242; 2012.
[10] Dayal, S.; Lentz, S. R. ADMA and hyperhomocysteinemia. Vasc Med 10 Suppl 1:S27-33; 2005.
[11] Campesi, I.; Carru, C.; Zinellu, A.; Occhioni, S.; Sanna, M.; Palermo, M.; et al. Regular cigarette smoking influences the transsulfuration pathway, endothelial function, and inflammation biomarkers in a sex-gender specific manner in healthy young humans. Am J Transl Res 5:497-509; 2013.
[12] Semba, R. D.; Ferrucci, L.; Sun, K.; Walston, J.; Varadhan, R.; Guralnik, J. M.; et al. Oxidative stress is associated with greater mortality in older women living in the community. J Am Geriatr Soc 55:1421-1425; 2007.
[13] Michos, E. D.; Vasamreddy, C. R.; Becker, D. M.; Yanek, L. R.; Moy, T. F.; Fishman, E. K.; et al. Women with a low Framingham risk score and a family history of premature coronary heart disease have a high prevalence of subclinical coronary atherosclerosis. Am Heart J 150:1276-1281; 2005.
[14] Beal, M. F. Oxidatively modified proteins in aging and disease. Free Radic Biol Med 32:797-803; 2002.
[15] Chevion, M.; Berenshtein, E.; Stadtman, E. R. Human studies related to protein oxidation: protein carbonyl content as a marker of damage. Free Radic Res 33 Suppl:S99-108; 2000.
[16] Tomasina, F.; Carabio, C.; Celano, L.; Thomson, L. Analysis of two methods to evaluate antioxidants. Biochemistry and molecular biology education: Biochem Mol Biol Educ 40:266-270; 2012.
[17] Benzie, I. F.; Strain, J. J. The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay. Anal Biochem 239:70-76; 1996.
[18] Friedewald, W. T.; Levy, R. I.; Fredrickson, D. S. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 18:499-502; 1972.
[19] Fields, R.; Dixon, H. B. Micro method for determination of reactive carbonyl groups in proteins and peptides, using 2,4-dinitrophenylhydrazine. Biochem J 121:587-589; 1971.
[20] Levine, R. L.; Garland, D.; Oliver, C. N.; Amici, A.; Climent, I.; Lenz, A. G.; Ahn, B. W.; Shaltiel, S.; Stadtman, E. R. Determination of carbonyl content in oxidatively modified proteins. Methods Enzymol 186:464-478; 1990.
[21] Huang, D.; Ou, B.; Prior, R. L. The chemistry behind antioxidant capacity assays. J Agric Food Chem 53:1841-1856; 2005.
[22] Konhilas, J. P. What we know and do not know about sex and cardiac disease. J Biomed Biotechnol 2010:562051; 2010.
[23] Meagher, E. A. Addressing cardiovascular disease in women: focus on dyslipidemia. J Am Board Fam Pract 17:424-437; 2004.
[24] Mittendorfer, B. Sexual dimorphism in human lipid metabolism. J Nutr 135:681-686; 2005.
[25] Yunoki, K.; Naruko, T.; Inaba, M.; Inoue, T.; Nakagawa, M.; Sugioka, K.; et al. Gender-specific correlation between plasma myeloperoxidase levels and serum high-density lipoprotein-associated paraoxonase-1 levels in patients with stable and unstable coronary artery disease. Atherosclerosis 231:308-314, 2013.
[26] Domingues RM, Domingues P, Melo T, Pérez-Sala D, Reis A, Spickett CM Lipoxidation adducts with peptides and proteins: Deleterious modifications or signaling mechanisms? J Proteomics. 92:110-31; 2013.
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  • APA Style

    Laura Celano, Anabel Vidal, Alicia Olascoaga, Walter Alallon, Ana Denicola, et al. (2013). Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men. American Journal of Clinical and Experimental Medicine, 1(3), 53-57. https://doi.org/10.11648/j.ajcem.20130103.13

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    ACS Style

    Laura Celano; Anabel Vidal; Alicia Olascoaga; Walter Alallon; Ana Denicola, et al. Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men. Am. J. Clin. Exp. Med. 2013, 1(3), 53-57. doi: 10.11648/j.ajcem.20130103.13

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    AMA Style

    Laura Celano, Anabel Vidal, Alicia Olascoaga, Walter Alallon, Ana Denicola, et al. Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men. Am J Clin Exp Med. 2013;1(3):53-57. doi: 10.11648/j.ajcem.20130103.13

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  • @article{10.11648/j.ajcem.20130103.13,
      author = {Laura Celano and Anabel Vidal and Alicia Olascoaga and Walter Alallon and Ana Denicola and Leonor Thomson},
      title = {Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men},
      journal = {American Journal of Clinical and Experimental Medicine},
      volume = {1},
      number = {3},
      pages = {53-57},
      doi = {10.11648/j.ajcem.20130103.13},
      url = {https://doi.org/10.11648/j.ajcem.20130103.13},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20130103.13},
      abstract = {Profuse epidemiological evidence supports a higher risk for coronary heart disease and stroke in smoker women than in men with the same habit. Although it is already known that cigarette smoking alters the redox state, is unknown if the imbalance in the normal equilibrium between oxidants and antioxidants is responsible for the elevated female susceptibility. Therefore, the aim of this work was to estimate the effect of smoking on serum redox status in women compared with men, accounting for divergences in other major risk factors for cardiovascular disease. Lipid profile, antioxidant capacity, and serum carbonyls were assessed in 116 healthy Uruguayans, composed by 50 females and 66 males. The smoking habit was declared by 17 females (34 %) and 36 males (54 %). The lipid profile was modified by cigarette smoking, affecting in a different way males and females. In particular, HDL-C that was higher in non-smoker females (59 (28) mg/dL) than in non-smoker males (46 (14) mg/dL) significantly decreased in smoker females (51 (13) mg/dL), remaining unchanged in the smoker male population (42 (12) mg/dL). Conversely LDL-C, which gave similar values for non-smoker females (110.1 ± 35.2 mg/dL) and males (98.5 ± 36.0 mg/dL), increased exclusively in smoker males (122.2 ± 36.4 mg/dL, p<0.05). In turn, the level of serum antioxidants that was higher in non-smoker males (1.9  0.3 mM FRAP) than females (1.5  0.4 mM /FRAP), remained unchanged in smokers. Similar results were obtained for carbonyls, which showed higher levels in non-smoker males (0.90 ± 0.32 nmol/mg of protein) than females (0.74 ± 0.32 nmol/mg of protein), and while the level remained unmodified in smokers males (0.86  0.28 nmol/mg of protein) increased non-significantly in smoker females (0.79  0.31 nmol/mg of protein). Whereas the oxidation index correlated positively with LDL-C (r = 0.45) in smoker males, and with triglycerides in both non-smoker and smoker females(r = 0.42 and 0.79, respectively), a negative and intense correlation with HDL-C (r = -0.79), and a positive one with the LDL-C/HDL-C index (r = 0.87) was observed exclusively in smoker females. Our results point to an association at the molecular level between oxidative stress footprints and plasma lipoprotein/cholesterol concentration predominantly in smoker females, and support the concept that the higher sensitivity of women to smoking related cardiovascular pathology is associated with oxidants-mediated biomolecular insults.},
     year = {2013}
    }
    

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  • TY  - JOUR
    T1  - Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men
    AU  - Laura Celano
    AU  - Anabel Vidal
    AU  - Alicia Olascoaga
    AU  - Walter Alallon
    AU  - Ana Denicola
    AU  - Leonor Thomson
    Y1  - 2013/12/30
    PY  - 2013
    N1  - https://doi.org/10.11648/j.ajcem.20130103.13
    DO  - 10.11648/j.ajcem.20130103.13
    T2  - American Journal of Clinical and Experimental Medicine
    JF  - American Journal of Clinical and Experimental Medicine
    JO  - American Journal of Clinical and Experimental Medicine
    SP  - 53
    EP  - 57
    PB  - Science Publishing Group
    SN  - 2330-8133
    UR  - https://doi.org/10.11648/j.ajcem.20130103.13
    AB  - Profuse epidemiological evidence supports a higher risk for coronary heart disease and stroke in smoker women than in men with the same habit. Although it is already known that cigarette smoking alters the redox state, is unknown if the imbalance in the normal equilibrium between oxidants and antioxidants is responsible for the elevated female susceptibility. Therefore, the aim of this work was to estimate the effect of smoking on serum redox status in women compared with men, accounting for divergences in other major risk factors for cardiovascular disease. Lipid profile, antioxidant capacity, and serum carbonyls were assessed in 116 healthy Uruguayans, composed by 50 females and 66 males. The smoking habit was declared by 17 females (34 %) and 36 males (54 %). The lipid profile was modified by cigarette smoking, affecting in a different way males and females. In particular, HDL-C that was higher in non-smoker females (59 (28) mg/dL) than in non-smoker males (46 (14) mg/dL) significantly decreased in smoker females (51 (13) mg/dL), remaining unchanged in the smoker male population (42 (12) mg/dL). Conversely LDL-C, which gave similar values for non-smoker females (110.1 ± 35.2 mg/dL) and males (98.5 ± 36.0 mg/dL), increased exclusively in smoker males (122.2 ± 36.4 mg/dL, p<0.05). In turn, the level of serum antioxidants that was higher in non-smoker males (1.9  0.3 mM FRAP) than females (1.5  0.4 mM /FRAP), remained unchanged in smokers. Similar results were obtained for carbonyls, which showed higher levels in non-smoker males (0.90 ± 0.32 nmol/mg of protein) than females (0.74 ± 0.32 nmol/mg of protein), and while the level remained unmodified in smokers males (0.86  0.28 nmol/mg of protein) increased non-significantly in smoker females (0.79  0.31 nmol/mg of protein). Whereas the oxidation index correlated positively with LDL-C (r = 0.45) in smoker males, and with triglycerides in both non-smoker and smoker females(r = 0.42 and 0.79, respectively), a negative and intense correlation with HDL-C (r = -0.79), and a positive one with the LDL-C/HDL-C index (r = 0.87) was observed exclusively in smoker females. Our results point to an association at the molecular level between oxidative stress footprints and plasma lipoprotein/cholesterol concentration predominantly in smoker females, and support the concept that the higher sensitivity of women to smoking related cardiovascular pathology is associated with oxidants-mediated biomolecular insults.
    VL  - 1
    IS  - 3
    ER  - 

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Author Information
  • Enzimología, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay

  • Enzimología, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay

  • Laboratorio Clínico, Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay

  • Laboratorio Clínico, Hospital de Clínicas, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay

  • Center for Free Radicals and Biomedical Research, CEINBIO, Universidad de la República, Montevideo, Uruguay

  • Enzimología, Facultad de Ciencias, Universidad de la República, Montevideo, Uruguay

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